XIST knockdown markedly repressed cell proliferation, migration and invasion and promoted the apoptosis of LSCC cells and the effects were antagonized by loss of miR-125b-5p. MiR-125b-5p was a target of XIST in LSCC cells, and it could bind to TRIB2 as well. Moreover, XIST-loss-induced downregulation of TRIB2 could be significantly reversed by miR-125b-5p knockdown. XIST promoted the growth of LSCC tumor in vivo. CONCLUSION LncRNA XIST promoted the malignance of LSCC cells partly through competitively binding to miR-125b-5p, which in turn increased TRIB2 expression. Copyright 2020 The Author(s).BACKGROUND Previous studies have demonstrated some associations between dietary vitamin A intake and ovarian cancer risk with an inconsistent relationship. We therefore performed this study to further explore the association between them. METHODS Databases of PubMed, Embase, and Web of Science were retrieved up to September 1, 2019. Summarized relative risk (RR) with corresponding 95% confidence intervals (CI) were calculated. Stata 14.0 software was used for data analysis. RESULTS Fifteen articles involving 4,882 cases and 443,179 participants were included in this meta-analysis. A positive association between dietary vitamin A intake and ovarian cancer risk was found (RR=0.816, 95%CI= 0.723-0.920, I2= 48.4%, Pfor heterogeneity= 0.019). Significant association was also found in case-control studies (RR=0.769, 95%CI= 0.655-0.902), but not in cohort studies. When we performed the analysis between ovarian cancer risk and geographic locations, we found an inverse association in North American populations (RR=0.825, 95%CI= 0.720-0.946), instead of other populations. CONCLUSIONS In summary, findings from this study suggested that higher dietary intake of vitamin A may contribute to the lower development of ovarian cancer, especially among North Americans. Copyright 2020 The Author(s).BACKGROUND Approximately 40% of all Enterobacterales (EB) bloodstream infections (BSI) among solid organ transplant recipients (SOTR) are due to extended-spectrum beta-lactamase (ESBL)-producing organisms, but risk factors for such infections remain ill-defined in this population. Thus, we sought to determine the risk factors for ESBL-EB BSI among SOTR. METHODS A multicenter case-control study was performed. All SOTR with an EB BSI at the Hospital of the University of Pennsylvania and University of Maryland Medical Center between January 1, 2007 and June 30, 2018, and at The Johns Hopkins Hospital between January 1, 2005 and December 31, 2015, were included. Cases were those with an ESBL-EB BSI. Controls were those with a non-ESBL-EB BSI. Multivariable logistic regression was performed to determine risk factors for ESBL-EB BSI. RESULTS There were 988 episodes of EB BSI, of which 395 (40%) were due to an ESBL-EB. On multivariable analysis, the independent risk factors for ESBL-EB BSI included ESBL-EB on prior culture (aOR 12.75, 95% CI 3.23-50.33, P less then 0.001); a corticosteroid-containing immunosuppression regimen (aOR 1.30, 95% CI 1.03-1.65, P=0.030); acute rejection treated with corticosteroids (aOR 1.18, 95% CI 1.16-1.19, P less then 0.001); and exposure to third-generation cephalosporins (aOR 1.95, 95% CI 1.48-2.57, P less then 0.001), echinocandins (aOR 1.61, 95% CI 1.08-2.40, P=0.020), and trimethoprim-sulfamethoxazole (aOR 1.35, 95% CI 1.10-1.64, P=0.003). CONCLUSIONS We identified several novel risk factors that are uniquely important to the SOTR population, including exposure to trimethoprim-sulfamethoxazole and corticosteroid-containing immunosuppressive regimens. Further studies exploring these associations and testing interventions aimed at these modifiable risk factors among SOTR are needed. © The Author(s) 2020. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail journals.permissions@oup.com.Colorectal cancer (CRC) is the third most common malignancy and one of the leading causes of cancer-related death among men worldwide. CRC is a multifactor digestive pathology, which is a huge problem faced not only by clinicians but also by researchers. Importantly, a unique feature of CRC is the dysregulation of molecular signaling pathways. To date, a series of reviews have indicated that different signaling pathways are disordered and have potential as therapeutic targets in CRC. Nevertheless, an overview of the function and interaction of multiple signaling pathways in CRC is needed. Therefore, we summarized the pathways, biological functions and important interactions involved in CRC. First, we investigated the involvement of signaling pathways, including Wnt, PI3K/Akt, Hedgehog, ErbB, RHOA, Notch, BMP, Hippo, AMPK, NF-κB, MAPK and JNK. Subsequently, we discussed the biological function of these pathways in pathophysiological aspects of CRC, such as proliferation, apoptosis and metastasis. Finally, we summarized important interactions among these pathways in CRC. https://www.selleckchem.com/products/Phenformin-hydrochloride.html We believe that the interaction of these pathways could provide new strategies for the treatment of CRC. © 2020 The Author(s).Glycans are known to be involved in many biological processes, while little is known about the expression of N-glycans during vertebrate development. We now report the first quantitative studies of both the expression of N-linked glycans at six early development stages and the expression of N-glycosylated peptides at two early development stages in Xenopus laevis, the African clawed frog. N-Glycans were labeled with isobaric tandem mass tags, pooled, separated by capillary electrophoresis, and characterized using tandem mass spectrometry. We quantified 110 N-glycan compositions that spanned four orders of magnitude in abundance. Capillary electrophoresis was particularly useful in identifying charged glycans; over 40% of the observed glycan compositions were sialylated. The glycan expression was relatively constant until the gastrula-neurula transition (developmental stage 13), followed by massive reprogramming. An increase in oligomannosidic and a decrease in the paucimannosidic and phosphorylated oligomannosidic glycans were observed at the late tailbud stage (developmental stage 41).